Ruxolitinib (RUX) cream 1.5%, a selective Janus kinase (JAK) 1 and 2 inhibitor initially developed for myelofibrosis, has emerged as a novel therapeutic agent in dermatology. It is the first topical JAK inhibitor approved by the Food and Drug Administration for atopic dermatitis (AD) and non-segmental vitiligo. This article reviews the pharmacological profile, mechanism of action, and clinical efficacy of topical RUX in immune-mediated skin conditions. RUX inhibits cytokine-induced JAK-signal transducer and activator of transcription signaling, reducing inflammation and pruritus with minimal systemic absorption and a favorable safety profile. In phase III TRuE-AD1/AD2 trials, RUX demonstrated significant improvements in the investigator’s global assessment, eczema area and severity index scores, and pruritus in patients with mild-to-moderate AD. Similarly, in the TRuE-V1/V2 studies for vitiligo, RUX achieved superior rates of facial vitiligo area scoring index (F-VASI75) and other repigmentation measures compared to vehicle, with sustained benefits at week 52. Common adverse effects included application site reactions such as burning, acne, and pruritus. Beyond its approved indications, emerging evidence supports off-label use in conditions such as lichen planus, alopecia areata, and cutaneous lupus, among others. While preliminary data suggest a positive impact on the skin microbiome, further studies are warranted. RUX cream represents a promising advancement in targeted dermatological therapy, offering localized efficacy with minimal systemic risk.
Datta et al. (2026) studied this question.